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Signals for the remodeling of the cardiac interstitium in systemic hypertension
K T Weber1, C G Brilla, J S Janicki
1Division of Cardiology, University of Missouri-Columbia 65212.
Insights
Myocardial hypertrophy involves cardiomyocyte growth, but nonmyocyte growth can vary. This study investigated how hemodynamic and hormonal factors influence ventricular mass and collagen in hypertension models.
Area of Science:
- Cardiovascular Biology
- Cardiac Physiology
- Hypertension Research
Background:
- Myocardial hypertrophy is characterized by cardiomyocyte growth, but nonmyocyte involvement can lead to heterogeneous tissue remodeling.
- The relative contributions of hemodynamic and hormonal factors to this process are not fully understood.
Purpose of the Study:
- To investigate the independent roles of hemodynamic and hormonal factors in cardiac hypertrophy and collagen accumulation.
- To compare these effects across different models of arterial hypertension in rats.
Main Methods:
- Utilized three rat models of arterial hypertension: renovascular hypertension (RHT), infrarenal aorta banding (IRB), and chronic aldosterone (ALDO) administration.
- Compared ventricular mass and cardiac fibroblast collagen accumulation under varying levels of arterial pressure, angiotensin II (Ang II), and ALDO.
Main Results:
- Hemodynamic and hormonal factors differentially regulate ventricular mass and collagen deposition.
- Specific hormonal profiles (e.g., elevated Ang II and ALDO in RHT) correlated with distinct hypertrophic and fibrotic responses.
Conclusions:
- Cardiac hypertrophy is not a uniform process and can be influenced by independent hemodynamic and hormonal signaling pathways.
- Understanding these distinct pathways is crucial for targeted therapeutic strategies in hypertensive heart disease.
Abstract:
Cardiac myocyte growth is the common denominator in myocardial hypertrophy irrespective of the hypertrophic stimulus. The hypertrophic remodeling of the myocardium may or may not also include the growth of nonmyocyte cells, thereby creating the potential for heterogeneity in tissue growth. Hypertrophy, therefore, need not be a uniform process, especially if trophic factors responsible for myocyte and nonmyocyte growth are independent of one another. To examine this hypothesis further, we determined the relative importance of hemodynamic and hormonal factors in augmenting ventricular mass and cardiac fibroblast-induced collagen accumulation in several rat (Sprague-Dawley) models of arterial hypertension: renovascular hypertension (RHT), infrarenal aorta banding (IRB), and chronic aldosterone (ALDO) administration. Elevations in arterial pressure were comparable in each, whereas circulating angiotension II (Ang II) and ALDO were dissimilar: in RHT, each was increased; with IRB they were normal; and with chronic ALDO, Ang II was suppressed whereas ALDO was increased. We reasoned that because of the in-series arrangement of the ventricles, where only the left ventricle (LV) experienced an elevation in systolic pressure, the right ventricle (RV) served as a negative control regarding hemodynamic factors. Relative to the in-parallel arrangement of the ventricles, provided by the coronary circulation, the RV served as a positive control for circulating hormones.(ABSTRACT TRUNCATED AT 250 WORDS)